Comparing the physiological cost of step-powered video gaming, sedentary video gaming and self paced ambulatory activity in university students

Objectives: Methods for converting inactive video gaming to active video gaming have gained popularity in recent years. This study compared the physiological cost of a new peripheral device that used steps to power video gaming in an interactive manner against sedentary video gaming and self-paced ambulatory activity of university students (aged 19-29 years).Methods: Nineteen adults (9 male, 10 female) performed six 10-minute activities, namely self-paced leisurely walking, self-paced brisk walking, self-paced jogging, two forms of sedentary video gaming, and step-powered video gaming. Activities were performed in a random order. Physiological cost during the activities was measured using Actiheart.Results: Energy expenditure during step-powered video gaming (388.8 kcal.h-1) was comparable to the energy expended during brisk walking (373.8 kcal.h-1), and elicited a higher energy cost than sedentary video gaming (124.1 kcal.h-1) but a lower energy cost than jogging (694.5 kcal.h-1).Conclusion: Overall, step-powered video gaming could be used as an entertaining and appealing tool to increase physical activity, though it should not be used as a complete substitute for traditional exercise, such as jogging.<br /

Lipid Anti-Lipid Antibody Responses Correlate with Disease Activity in Systemic Lupus Erythematosus

10.1371/journal.pone.0055639PLoS ONE82

Rural EV charging: The effects of charging behaviour and electricity tariffs

As with many socio-techno transitions, rural areas often get left behind and Electric Vehicles (EVs) are no exception. This paper aims to highlight the lack of academic discourse surrounding the transition to EVs for rural areas as well as presenting the modelling and results of several potential scenarios for rural EV charging habits. Utilising 7-day travel patterns for a small rural village in the Peak District National Park, UK, this paper investigates the energy requirements and potential recharging patterns should this settlement switch all vehicles to EVs. Two key parameters have been incorporated into the EV charging model; electricity tariffs and charging behaviour based on current battery State of Charge (SoC). The model simulated a 4 week period, from which a time period, with a minimum length of one week, where energy balance could be assured for the whole system was extracted. Results show that instantaneous energy and power requirements can vary drastically depending on electricity tariffs and charging behaviours which could be a major cause for concern for rural grid infrastructure, and for the larger EV transition across the UK

Donor cytokine genotype influences the development of acute rejection after renal transplantation

Background. Acute allograft rejection remains an important cause of morbidity after kidney transplantation, and has been shown to be a crucial determinant of long-term graft function. Although rejection is mediated by recipient lymphocytes, both donor and recipient factors contribute to the local environment that influences the nature, severity, and duration of the rejection response. Cytokines are a major determinant of this milieu, and this study sought to explore the impact of donor cytokine and cytokine receptor gene polymorphisms on acute rejection after renal transplantation. Methods. A total of 145 cadaveric renal allograft donors were selected for analysis according to the presence or absence of graft rejection in the first 30 days after transplantation. DNA was genotyped for 20 polymorphisms in 11 cytokine and cytokine receptor genes using the polymerase chain reaction with sequence specific primers. Associations were assessed using contingency table analysis and the χ2 test, using a two-set design. Results. A polymorphism at position -174 of the donor IL-6 gene was associated with the incidence (P =0.0002) and severity (P =0.000007) of recipient acute rejection. This finding was independent of HLA-DR matching. Acute rejection was not influenced by recipient IL-6 genotype, or by donor-recipient matching of IL-6 genotype. Conclusion. This study identifies donor IL-6 genotype as a major genetic risk factor for the development of acute rejection after renal transplantation. This provides evidence that donor-derived cytokines play a major role in determining outcome after transplantation, and will contribute to the development of therapeutic algorithms to predict individuals at particularly high risk of acute rejection

Leucocyte subset-specific type 1 interferon signatures in SLE and other immune-mediated diseases

10.1136/rmdopen-2015-000183RMD Open21e00018

A type I interferon transcriptional signature precedes autoimmunity in children genetically at risk of type 1 diabetes.

Diagnosis of the autoimmune disease type 1 diabetes (T1D) is preceded by the appearance of circulating autoantibodies to pancreatic islets. However, almost nothing is known about events leading to this islet autoimmunity. Previous epidemiological and genetic data have associated viral infections and anti-viral type I interferon (IFN) immune response genes with T1D. Here, we first used DNA microarray analysis to identify IFN-&beta; inducible genes in vitro and then used this set of genes to define an IFN-inducible transcriptional signature in peripheral blood mononuclear cells from a group of active systemic lupus erythematosus patients (N=25). Using this predefined set of 225 IFN signature genes, we investigated expression of the signature in cohorts of healthy controls (N=87), T1D patients (N=64) and a large longitudinal birth cohort of children genetically predisposed to T1D (N=109; 454 microarrayed samples). Expression of the IFN signature was increased in genetically-predisposed children prior to the development of autoantibodies (P=0.0012), but not in established T1D patients. Upregulation of IFN-inducible genes was transient, temporally associated with a recent history of upper respiratory tract infections (P=0.0064) and marked by increased expression of SIGLEC-1 (CD169), a lectin-like receptor expressed on CD14(+) monocytes. DNA variation in IFN-inducible genes altered T1D risk (P=0.007), as exemplified by IFIH1, one of the genes in our IFN signature and for which increased expression is a known disease risk factor. These findings identify transient increased expression of type I IFN genes in pre-clinical diabetes as a risk factor for autoimmunity in children with a genetic predisposition to T1D

Mechanisms of Resistance to EGFR Inhibition Reveal Metabolic Vulnerabilities in Human GBM.

Amplification of the epidermal growth factor receptor gene (EGFR) represents one of the most commonly observed genetic lesions in glioblastoma (GBM); however, therapies targeting this signaling pathway have failed clinically. Here, using human tumors, primary patient-derived xenografts (PDX), and a murine model for GBM, we demonstrate that EGFR inhibition leads to increased invasion of tumor cells. Further, EGFR inhibitor-treated GBM demonstrates altered oxidative stress, with increased lipid peroxidation, and generation of toxic lipid peroxidation products. A tumor cell subpopulation with elevated aldehyde dehydrogenase (ALDH) levels was determined to comprise a significant proportion of the invasive cells observed in EGFR inhibitor-treated GBM. Our analysis of the ALDH1A1 protein in newly diagnosed GBM revealed detectable ALDH1A1 expression in 69% (35/51) of the cases, but in relatively low percentages of tumor cells. Analysis of paired human GBM before and after EGFR inhibitor therapy showed an increase in ALDH1A1 expression in EGFR-amplified tumors (P &lt; 0.05, n = 13 tumor pairs), and in murine GBM ALDH1A1-high clones were more resistant to EGFR inhibition than ALDH1A1-low clones. Our data identify ALDH levels as a biomarker of GBM cells with high invasive potential, altered oxidative stress, and resistance to EGFR inhibition, and reveal a therapeutic target whose inhibition should limit GBM invasion